Key result
Atrial fibrillation significantly reduced H2S levels and cystathionine-y-lyase expression while increasing the Warburg effect, endoplasmic reticulum stress, and atrial fibrosis compared to sinus rhythm.
Why the study?
The specific mechanism by which hydrogen sulfide improves the progression of atrial fibrosis to AF remains unclear.
Does hydrogen sulfide supplementation prevent Angiotensin II-induced atrial fibrosis and atrial fibrillation in preclinical models?
Case-Control (n=12)
No
Does hydrogen sulfide supplementation prevent Angiotensin II-induced atrial fibrosis and atrial fibrillation in preclinical models?
Hydrogen sulfide supplementation ameliorates Angiotensin II-induced atrial fibrosis and atrial fibrillation by inhibiting the Warburg effect and endoplasmic reticulum stress in preclinical models.
Answers are grounded in this paper and cite their sources.
Lower H2S linked to human atrial fibrosis; leaves open whether supplementation alters AF progression or outcomes.
Atrial fibrosis is the basis for the occurrence and development of atrial fibrillation (AF) and is closely related to the Warburg effect, endoplasmic reticulum stress (ERS) and mitochondrion dysfunctions-induced cardiomyocyte apoptosis. Hydrogen sulfide (H 2 S) is a gaseous signalling molecule with cardioprotective, anti-myocardial fibrosis and improved energy metabolism effects. Nevertheless, the specific mechanism by which H 2 S improves the progression of atrial fibrosis to AF remains unclear. A case-control study of patients with and without AF was designed to assess changes in H 2 S, the Warburg effect, and ERS in AF. The results showed that AF can significantly reduce cystathionine- γ -lyase (CSE) and 3-mercaptopyruvate thiotransferase (3-MST) expression and the H 2 S level, induce cystathionine- β -synthase (CBS) expression; increase the Warburg effect, ERS and atrial fibrosis; and promote left atrial dysfunction. In addition, AngII-treated SD rats had an increased Warburg effect and ERS levels and enhanced atrial fibrosis progression to AF compared to wild-type SD rats, and these conditions were reversed by sodium hydrosulfide (NaHS), dichloroacetic acid (DCA) or 4-phenylbutyric acid (4-PBA) supplementation. Finally, low CSE levels in AngII-induced HL-1 cells were concentration- and time-dependent and associated with mitochondrial dysfunction, apoptosis, the Warburg effect and ERS, and these effects were reversed by NaHS, DCA or 4-PBA supplementation. Our research indicates that H 2 S can regulate the AngII-induced Warburg effect and ERS and might be a potential therapeutic drug to inhibit atrial fibrosis progression to AF.
No takes yet. Share an insight, caveat, or question.
Hu et al. (2021) conducted a case-control in Atrial Fibrillation in Rheumatic Heart Disease (n=12). Atrial fibrillation vs. Sinus rhythm was evaluated on Atrial tissue H2S levels and expression of Warburg effect and endoplasmic reticulum stress markers. Atrial fibrillation significantly reduced H2S levels and cystathionine-y-lyase expression while increasing the Warburg effect, endoplasmic reticulum stress, and atrial fibrosis compared to sinus rhythm.
Synapse has enriched 10 related papers. Consider them for comparative context: